Nonpathological Changes Research Articles

Age Related Motor-Unit Remodeling and Its Effect on Muscle Performance

A ging is associated with loss of muscle mass and strength as a result of numerous nonpathological changes within the neuromuscular system. Two commonly reported changes include loss of fiber number and size; however, these factors alone fail to account adequately for the magnitude of strength loss (21). Despite detailed observations and quantification of declining strength and mass, the underlying mechanisms precipitating such changes are not fully understood. Neurologic degeneration offers a plausible explanation to account for such changes.

Neurons, glia, and plasticity in normal brain aging

Early manifestations of brain aging have received much less attention than the drastic degeneration of AD and MID. During nonpathological changes of normal aging, brain systems differ in the involvement of neuron loss. Spatial learning can become impaired without evidence for neuron loss, whereas eye-blink conditioning deficits are well correlated with Purkinje neuron loss. Glial activation, in particular the increased expression of glial fibrillary acidic protein (GFAP), may be a factor in impaired synaptic plasticity. Lastly, it is discussed how developmental variations in the numbers of Purkinje cells and ovarian oocytes can be factors in outcomes of aging that are not under strict genetic control.

Mesostriatal dopamine markers in aged Long-Evans rats with sensorimotor impairment

Changes in the mesostriatal dopamine system associated with normal aging are observed in both human and laboratory animals, but the specific behavioral consequences of these nonpathological changes are largely unexplored. The present study (a) assessed the effects of normal aging on markers for the mesostriatal dopamine system, and (b) examined the relationship of age-related changes in this system to decline in reaction time performance. Decreased levels of midbrain dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) were observed in the aged rats as compared to young, but there was no evidence for age-related changes in the density of D 1 or D 2 receptor binding or the density of dopamine uptake sites. Some differences were observed when the aged rats were grouped according to reaction time performance. Aged RT-unimpaired rats exhibited higher density of D 1 binding in rostrodorsal striatal patch areas, but lower overall levels of DA. In caudal striatum, aged RT-unimpaired rats exhibited lower DA and higher DOPAC levels.